Effect of histamine on motor function of opossum sphincter of Oddi

1981 ◽  
Vol 241 (2) ◽  
pp. G122-G128 ◽  
Author(s):  
J. Toouli ◽  
W. J. Dodds ◽  
R. Honda ◽  
W. J. Hogan
Keyword(s):  
Smooth Muscle ◽  
Motor Function ◽  
Large Dose ◽  
Contractile Activity ◽  
Sphincter Of Oddi ◽  
Inhibitory Effect ◽  
Excitatory Effect ◽  
Catheter System ◽  
Infused Catheter System ◽  
Stimulation Of

In this study, we evaluated the effect of histamine on phasic contractile activity in the opossum sphincter of Oddi (SO). SO manometry was done in 35 animals, using an infused catheter system with minimal compliance. In anesthetized animals, phasic SO contractions occurred at a frequency of 7.3 +/- 0.3 (SE) contractions/min with an amplitude of 83 +/- 4 mmHg. Intravenous histamine (5-80 micrograms/kg) invariably inhibited the frequency and amplitude of SO phasic contractions. At larger doses, the SO contractions were abolished for several minutes. The SO inhibitory effect of histamine was duplicated by the selective H1-agonist, 2-pyridylethylamine, and abolished by H1-blockade with pyrilamine or neural blockade with tetrodotoxin. After tetrodotoxin, histamine and 2-pyridylethylamine caused an increased frequency and amplitude of SO contractions. This excitatory effect was blocked by pyrilamine. The histamine effects on SO phasic contractions were not altered by metiamide, atropine, phentolamine, propranolol, hexamethonium, or a large dose of nicotine. We conclude that 1) histamine depresses phasic SO contractions in the opossum; 2) histamine's depressant SO effect is mediated by H1 stimulation of noncholinergic, nonadrenergic SO inhibitory nerves, overriding an H1 stimulatory effect on SO smooth muscle; and 3) histamine has no H2-mediated effect on the opossum SO.

scholarly journals Afferent Stochastic Modulation of Crayfish Caudal Photoreceptor Units

1968 ◽  
Vol 51 (4) ◽  
pp. 534-551 ◽  
Author(s):  
Howard T. Hermann ◽  
Richard E. Olsen
Keyword(s):  
Inhibitory Effect ◽  
Fiber Optic Probe ◽  
Inhibitory Effects ◽  
Excitatory Effect ◽  
Multiple Pulses ◽  
Caudal Photoreceptor ◽  
Stochastic Modulation ◽  
The Mean ◽  
Optic Probe ◽  
Stimulation Of

When all roots to the sixth ganglion of the crayfish are cut, the caudal photoreceptor unit (PRU) fires at regular intervals. With an intact preparation, stimulation of caudal tactile hairs has predominantly inhibitory effects on the PRU: short bursts of afferent impulses, produced by momentary mechanical stimulation of tactile hairs, have (a) occasional immediate excitatory effect on the PRU, (b) prolonged inhibitory effect. The mean firing rate of the afferented and deafferented PRUs reacts similarly to a step increase in light, but the same unit fires faster after deafferentation. In the dark, deafferented units often fire paired or multiple pulses; the interval between pulses in a pair is similar to the short mode in afferented histograms. A fiber-optic probe of the caudal ganglion demonstrates the approximate location of the photosensitive element.

Neurotensin inhibition of canine intestinal motility in vivo via α-adrenoceptors

1984 ◽  
Vol 62 (4) ◽  
pp. 403-411 ◽  
Author(s):  
Y. Sakai ◽  
E. E. Daniel ◽  
J. Jury ◽  
J. E. T. Fox
Keyword(s):  
Acetylcholine Release ◽  
Contractile Activity ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Maximal Inhibition ◽  
Contractile Responses ◽  
Adrenergic Antagonists ◽  
Distal Site ◽  
Stimulation Of

Neurotensin given intra-arterially in bolus doses to the canine small intestine inhibited field-stimulated, atropine-sensitive contractile responses in the duodenum (mean effective dose (ED50) = 3.2 × 10−11 mol) and in the ileum (mean ED50 = 2.1 × 10−11 mol). Norepinephrine (ED50 = 3 × 10−9 mol) also inhibited these contractile responses. Phenylephrine (ED50 = 1.3 × 10−8 mol) was one-fourth as potent as norepinephrine and clonidine (ED50 = 8 × 10−10 mol) was at least as potent as norepinephrine, while isoproterenol (up to 8 × 10−8 mol) failed to show any inhibitory effects. Phentolamine (2 mg/kg) increased significantly the ED50 of neurotensin and norepinephrine. Prazosin (2 mg/kg) increased significantly the ED50 of norepinephrine in the duodenum but had no effect on the ED50 of neurotensin. Yohimbine (2 mg/kg) increased the ED50 values of neurotensin and adrenergic agonists. Both neurotensin and norepinephrine in doses causing maximal inhibition of field-stimulated responses decreased (by 40 to 60%) contractile responses to 9 × 10−10 mol (approximately the intra-arterial ED50 dose) of acetylcholine. Reserpine pretreatment markedly diminished the inhibition of spontaneous or field-stimulated phasic contractions by distention or field stimulation of a distal site. Reserpine also diminished the ED50 for neurotensin from 1 × 10−11 to 2 × 10−11 mol (p < 0.02), but did not abolish neurotensin's inhibitory effect. Tetrodotoxin (10–15 μg, intra-arterially) increased the dose of neurotensin required to inhibit spontaneous activity in the ileum but after this toxin, as after adrenergic antagonists or reserpine, maximal inhibition could still be obtained. These results suggested that neurotensin inhibited contractile activity of canine intestine by acting on neural receptors to release norepinephrine. Norepinephrine activated primarily α2-adrenoceptors and ultimately inhibited acetylcholine release. Neurotensin also inhibited contractions by activating a second, less sensitive receptor on smooth muscle.

KCl evokes contraction of airway smooth muscle via activation of RhoA and Rho-kinase

2004 ◽  
Vol 287 (4) ◽  
pp. L852-L858 ◽  
Author(s):  
Luke J. Janssen ◽  
Tracy Tazzeo ◽  
Jianmin Zuo ◽  
Evi Pertens ◽  
Shaf Keshavjee
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Contractile Activity ◽  
Rho Kinase ◽  
Western Blots ◽  
Downstream Effector ◽  
Highly Sensitive ◽  
Voltage Dependent ◽  
Evoked Contractions ◽  
Stimulation Of

Airway smooth muscle (ASM) cells express voltage-dependent Ca2+ channels, primarily of the L-subtype. These may play a role in excitation-contraction coupling of ASM, although other signaling pathways may also contribute: one of these includes Rho and its downstream effector molecule Rho-associated kinase (ROCK). Although voltage-dependent Ca2+ influx and Rho/ROCK signaling have traditionally been viewed as entirely separate pathways, recent evidence in vascular smooth muscle suggest differently. In this study, we monitored contractile activity (muscle baths) in bronchial and/or tracheal preparations from the pig, cow, and human, and further examined Rho and ROCK activities (Western blots and kinase assays) and cytosolic levels of Ca2+ (fluo 4-based fluorimetry) in porcine tracheal myocytes. KCl evoked substantial contractions that were suppressed in tracheal preparations by removal of external Ca2+ or using the selective L-type Ca2+ channel blocker nifedipine; porcine bronchial preparations were much less sensitive, and bovine bronchi were essentially unaffected by 1 μM nifedipine. Surprisingly, KCl-evoked contractions were also highly sensitive to two structurally different ROCK inhibitors: Y-27632 and HA-1077. Furthermore, the inhibitory effects of nifedipine and of the ROCK inhibitors were not additive. KCl also caused marked stimulation of Rho and ROCK activities, and both these changes were suppressed by nifedipine or by removal of external Ca2+. KCl-induced elevation of [Ca2+]i was not affected by Y-27632 but was reversed by NiCl2 or by BAPTA-AM. We conclude that KCl acts in part through stimulation of Rho and ROCK, possibly secondary to voltage-dependent Ca2+ influx.

scholarly journals Androgens Induce Nongenomic Stimulation of Colonic Contractile Activity through Induction of Calcium Sensitization and Phosphorylation of LC20 and CPI-17

2010 ◽  
Vol 24 (5) ◽  
pp. 1007-1023 ◽  
Author(s):  
María C. González-Montelongo ◽  
Raquel Marín ◽  
Tomás Gómez ◽  
Jorge Marrero-Alonso ◽  
Mario Díaz
Keyword(s):  
Smooth Muscle ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Contractile Activity ◽  
Rho Kinase ◽  
Regulatory Subunit ◽  
Calcium Sensitization ◽  
Regulatory Myosin Light Chain ◽  
Rapid Activation ◽  
Stimulation Of

Abstract We show that androgens, testosterone and 5α-dihydrotestosterone (DHT), acutely (∼40 min) provoke the mechanical potentiation of spontaneous and agonist-induced contractile activity in mouse colonic longitudinal smooth muscle. The results using flutamide, finasteride, cycloheximide, and actinomycin D indicate that androgen-induced potentiation is dependent on androgen receptors, requires reduction of testosterone to DHT, and occurs independently of transcriptional and translational events. Using permeabilized colonic smooth muscle preparations, we could demonstrate that mechanical potentiation is entirely due to calcium sensitization of contractile machinery. In addition, DHT (10 nm) increased phosphorylation of both 20-kDa myosin light chain (LC20) [regulatory myosin light chain, (MLC)] and CPI-17 (an endogenous inhibitor of MLC phosphatase). Paralleling these findings, inhibition of Rho-associated Rho kinase (ROK) and/or protein kinase C (PKC) with, respectively, Y27632 and chelerythrine, prevented LC20 phosphorylation and abolished calcium sensitization. In addition, inhibition of ROK prevents CPI-17 phosphorylation, indicating that ROK is located upstream PKC-mediated CPI-17 modulation in the signalling cascade. Additionally, androgens induce a rapid activation of RhoA and its translocation to the plasma membrane to activate ROK. The results demonstrate that androgens induce sensitization of colonic smooth muscle to calcium through activation of ROK, which in turn, activates PKC to induce CPI-17 phosphorylation. Activation of this pathway induces a potent steady stimulation of LC20 by inhibiting MLC phosphatase and displacing the equilibrium of the regulatory subunit towards its phosphorylated state. This is the first demonstration that colonic smooth muscle is a physiological target for androgen hormones, and that androgens modulate force generation of smooth muscle contractile machinery through nongenomic calcium sensitization pathways.

Effects of oestradiol-17β and 5α-dihydrotestosterone on guinea-pig prostate smooth muscle cell proliferation and steroid receptor expression in vitro

1994 ◽  
Vol 140 (3) ◽  
pp. 373-383 ◽  
Author(s):  
C Ricciardelli ◽  
D J Horsfall ◽  
P J Sykes ◽  
V R Marshall ◽  
W D Tilley
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Dna Synthesis ◽  
Steroid Receptor ◽  
Inhibitory Effect ◽  
Cell Number ◽  
Mrna Levels ◽  
Plating Density ◽  
Stimulation Of

Abstract Smooth muscle cells (SMCs) are the major cellular component of the prostatic stroma. The aim of this study was to examine the effects of oestradiol-17β (OE2) and 5α-dihydrotestosterone (DHT) on the proliferation of guinea-pig prostate SMCs in vitro. OE2 stimulated SMC DNA synthesis at all concentrations examined. At a plating density of 3·0 × 104 cells/cm2, maximal incorporation of [3H]thymidine (136% of control) was observed after 36 h of treatment with 1 nmol OE2/l. At the same plating density, DHT had an inhibitory effect on SMC DNA synthesis, with maximal effects (73% of control) being observed 24 h after treatment with 1 nmol DHT/l. These effects of OE2 and DHT were prevented by co-incubation with specific steroid receptor antagonists. At a threefold lower plating density (1·0 × 104 cells/cm2), the maximal stimulatory and inhibitory effects of OE2 and DHT were delayed by approximately 24 and 12 h respectively. At the lower plating density, a biphasic effect of DHT was observed on DNA synthesis; DHT was both inhibitory and stimulatory. Maximal inhibition (71% of control) and maximal stimulation (168% of control) were observed after 36 and 134 h treatment with DHT respectively. At the lower plating density, longer term treatment of SMC cultures with OE2 and DHT also resulted in an increase in cell number. After 7 days of treatment with OE2 and DHT, cell number increased by 13% and 12% respectively. When OE, and DHT were added in combination, the short-term inhibitory effect of DHT on SMC DNA synthesis was dominant over the stimulatory effect of OE2. Treatment with DHT for 24 h significantly inhibited OE2-induced stimulation of [3H] thymidine incorporation, irrespective of the prior duration of OE2 treatment. At the lower plating density, OE2 also decreased oestrogen receptor (ER) mRNA levels to 38% of control levels after 24 h of treatment. ER mRNA levels remained repressed until 72 h after treatment with OE2, and returned to control values following 96 h of treatment. Both the androgen-induced inhibition and stimulation of DNA synthesis observed following treatment of SMCs with 1 nmol DHT/l were associated with a reduction in androgen receptor (AR) mRNA levels. At an intermediate time (i.e. 48 h after commencement of treatment with DHT) AR mRNA levels were increased more than twofold over control levels. The increase in AR mRNA levels at 48 h after DHT treatment only occurred in cells plated at the lower density, suggesting that this is an essential requirement for the longer term stimulation of prostatic SMC proliferation by DHT. Journal of Endocrinology (1994) 140, 373–383

Nitric oxide as putative nonadrenergic noncholinergic inhibitory transmitter in the opossum sphincter of Oddi

1993 ◽  
Vol 71 (7) ◽  
pp. 525-530 ◽  
Author(s):  
H. D. Allescher ◽  
S. Lu ◽  
E. E. Daniel ◽  
M. Classen
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Sphincter Of Oddi ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Inhibitory Response ◽  
Sphincter Muscle ◽  
Field Stimulation ◽  
Excitatory Effect ◽  
Electrical Field

The sphincter of Oddi has a typical nonadrenergic noncholinergic inhibitory innervation; however, the transmitter of this inhibition has not been identified. The aim of the present study was to evaluate whether metabolites of the L-arginine – nitric oxide synthase pathway mediate neural inhibition in the sphincter of Oddi of the opossum. Electrical field stimulation at various frequencies (3, 5, and 10 pulses/s), performed in the presence of guanethidine (10−6 M) to exclude adrenergic responses, caused a slight, but significant excitatory response of the sphincter of Oddi. The responses were more pronounced at the duodenal side of the sphincter of Oddi than on the hepatic side. When the electrical field stimulation was repeated after blockading muscarinic receptors, using atropine (10−6 M), a potent inhibitory response was obtained. The inhibitory response to each of the various stimulation parameters was similar. Addition of L-arginine methyl ester (L-NAME, 2 × 10−4 M) abolished and reversed the inhibitory effect of electrical field stimulation, resulting in a potent stimulatory effect. Higher frequencies (5 and 10 pulses/s) were more potent in causing a stimulatory response than lower frequencies (3 pulses/s). The excitatory effect of electrical field stimulation was blocked or reversed to inhibition when the amino acid L-arginine (2 × 10−3 M) was added to the bath. In a second series of experiments, the inhibitory effect of electrical field stimulation in the presence of atropine and guanethidine was not prevented after the addition of methylene blue (5 × 10−5 M), a substance that, in vascular smooth muscle, has been demonstrated to block cyclic GMP dependent inhibitory responses. These data demonstrate that the sphincter of Oddi is characterized by an excitatory innervation that is partly cholinergic and partly nonadrenergic noncholinergic (NANC), while the NANC inhibitory response of this sphincter muscle is mediated by the release of endogenous nitric oxide or related compounds.Key words: nonadrenergic, noncholinergic, nitric oxide, L-arginine, sphincter of Oddi, methylene blue.

The electrophysiological basis of the motor inhibitory effect of adrenaline on rabbit small intestinal smooth muscle

1976 ◽  
Vol 54 (4) ◽  
pp. 446-456 ◽  
Author(s):  
T. Y. El-Sharkawy ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Intestinal Motility ◽  
Inhibitory Effect ◽  
Intestinal Smooth Muscle ◽  
Control Potential ◽  
Control Activity ◽  
Small Intestinal ◽  
K Permeability ◽  
Stimulation Of

The spontaneous electrical activity of small intestinal smooth muscle cells consists of repetitive depolarizations (control activity) on which spikes (response activity) may be superimposed; each spike is preceded by a prepotential. Response activity is associated with contractions. Adrenaline initially abolished the response activity and any prepotentials, as well as the contractions, without altering the control activity or the membrane potential. This effect was followed by hyperpolarization and slight increase in the control potential amplitude. The hyperpolarization was insensitive to temperature (Q10 = 1.01) and was larger when the membrane was initially depolarized by K withdrawal but did not occur after the membrane was hyperpolarized by replacing Cl by propionate or by prolonged K withdrawal. It is suggested that adrenaline inhibits intestinal motility by uncoupling the control activity to response activity through suppression of the prepotentials. The adrenaline-induced hyperpolarization may be due to an increase in K permeability but not to stimulation of electrogenic Na pumping. The increase in K permeability may depend upon the presence of Cl ions.

scholarly journals Molecular mechanisms of ATP and insulin synergistic stimulation of coronary artery smooth muscle growth

2001 ◽  
Vol 280 (2) ◽  
pp. H795-H801 ◽  
Author(s):  
Yehenew M. Agazie ◽  
J. Courtney Bagot ◽  
Erica Trickey ◽  
Stephen P. Halenda ◽  
Peter A. Wilden
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Molecular Mechanisms ◽  
Muscle Growth ◽  
Inhibitory Effect ◽  
Akt Activation ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Artery Disease ◽  
Stimulation Of

Coronary artery disease (CAD) is the major cause of death in diabetics. Abnormal proliferation of coronary artery smooth muscle cells (CASMC) leads to intimal thickening in CAD. We examined signaling mechanisms involved in the mitogenic effect of ATP and insulin on CASMC. ATP and insulin individually stimulated DNA synthesis by 4- and 2-fold, respectively; however, they acted synergistically to stimulate an increase of 17-fold over basal. A similar synergistic stimulation of extracellular signal-regulated kinase (ERK) and mitogen-activated protein or ERK kinase activities was observed (ATP, 7-fold; insulin, 2-fold; and ATP + insulin, 16-fold over basal). However, the combination of ATP and insulin stimulated only an additive activation of Raf (ATP, 5-fold; insulin, <2-fold; and ATP + insulin, 8-fold over basal) and Ras (ATP, 5-fold; insulin, 2-fold; and ATP + insulin, 8-fold over basal). Thus convergence of ATP and insulin signals appears to be at the level of Ras and Raf. In addition, insulin stimulated activation of Akt (also known as protein kinase B) (10-fold over basal), whereas ATP had little effect. However, when ATP and insulin were added in combination, ATP dramatically reduced the insulin-stimulated Akt activation (2-fold above basal). Thus these results are consistent with ATP relieving an insulin-induced Akt-dependent inhibitory effect on the ERK signaling pathway, leading to synergistic stimulation of CASMC proliferation.

Prostaglandins and modulation of small bowel myoelectric activity

1992 ◽  
Vol 262 (3) ◽  
pp. G488-G497 ◽  
Author(s):  
C. T. Frantzides ◽  
E. A. Lianos ◽  
D. Wittmann ◽  
B. Greenwood ◽  
C. E. Edmiston
Keyword(s):  
Contractile Activity ◽  
Inhibitory Effect ◽  
Phase Iii ◽  
Myoelectric Activity ◽  
Dependent Manner ◽  
Excitatory Effect ◽  
Small Intestinal ◽  
Channel Dependent ◽  
Opposing Effects ◽  
Chronically Instrumented Dogs

We explored the effects of prostaglandins (PG) F2 alpha and E2 on the motor and myoelectric activity of the small intestine using closed intra-arterial injections in conscious chronically instrumented dogs. PGF2 alpha (0.125-5 micrograms) and PGE2 (1-10 micrograms) were injected via a T tube into a branch of the superior mesenteric artery perfusing a 15-cm segment of jejunum. Experiments were performed on four dogs in which the recording devices had been implanted above, below, and within the perfused segment. PGF2 alpha given during phase I of the migrating myoelectric complex cycle induced phasic contractions in the perfused segment of intestine in a dose-dependent manner. Atropine (50-100 micrograms), hexamethonium (15 mg), or TTX (10-15 micrograms) administered before the injection of PGF2 alpha failed to inhibit the effects of PGF2 alpha. In contrast pretreatment of the perfused segment with verapamil (2.5 mg) or PGE2 (1-5 micrograms) abolished the effects of PGF2 alpha. Moreover, PGE2 injected 5 min after the administration of PGF2 alpha inhibited the PGF2 alpha-induced contractions. Administration of PGE2 alone (3-10 micrograms) before the arrival of phase III activity in the perfused segment abolished phase III from this segment of intestine. Our studies indicate opposing effects of PGF2 alpha and PGE2 on small intestinal myoelectric and contractile activities. PGF2 alpha has a direct excitatory effect on the intestinal smooth muscle, which is calcium channel dependent but independent of intrinsic nerves. PGE2 has an inhibitory effect both on the spontaneous and PGF2 alpha-induced small intestinal myoelectric and contractile activity.

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